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1 ding mast cells, basophils, eosinophils, and type 2 innate lymphoid cells.
2 d with cutaneous expansion of IL-5-producing type 2 innate lymphoid cells.
3 lly associated invariant T (MAIT) cells, and type 2 innate lymphoid cells.
4 r innate immune cells, such as basophils and type 2 innate lymphoid cells.
5 his process to occur, even in the absence of type 2 innate lymphoid cells.
7 hopoietin) by colon tissues, which activated type 2 innate lymphoid cells and dendritic cells to prom
8 creased the numbers of eosinophils, IL-13(+) type 2 innate lymphoid cells and IL-13(+)CD4(+) T cells
10 okines IL-5 and IL-13 coming from Th2 cells, type 2 innate lymphoid cells, and probably mast cells.
11 sed in airway epithelial cells, macrophages, type 2 innate lymphoid cells, and TH2 cells along with i
12 the expansion of eosinophils, Th2 cells, and type 2 innate lymphoid cells, associated with an increas
13 +) lymphocytes, NK T cells, macrophages, and type 2 innate lymphoid cells compared with wild-type con
15 otently induces expansion of IL-13-producing type 2 innate lymphoid cells, correlating with airway co
16 f tuft cells, goblet cells, eosinophils, and type 2 innate lymphoid cells during parasite colonizatio
22 hanistically, we identify IL-13 release from type 2 innate lymphoid cells (ILC2) as sufficient to dri
24 rum IL-5 levels are maintained by long-lived type 2 innate lymphoid cells (ILC2) resident in peripher
29 at are associated with the expansion of lung type 2 innate lymphoid cells (ILC2s) and are dependent o
34 e we identified interleukin (IL)-9-producing type 2 innate lymphoid cells (ILC2s) as the mediators of
36 transiently expressed during development of type 2 innate lymphoid cells (ILC2s) but is not present
37 es is well established, the newly identified type 2 innate lymphoid cells (ILC2s) can also contribute
39 was inversely associated with the number of type 2 innate lymphoid cells (ILC2s) expressing IL-33Ral
40 ing ELISA, histology, and real-time PCR; and type 2 innate lymphoid cells (ILC2s) in lung single-cell
41 using murine models of allogeneic BMT, that type 2 innate lymphoid cells (ILC2s) in the lower GI tra
42 a previously undescribed deficit in c-Kit(+) type 2 innate lymphoid cells (ILC2s) in W/W(v) mice.
51 addition, the population of IL-13-secreting type 2 innate lymphoid cells (ILC2s) was expanded with r
55 Additionally, we cultured human T cells and type 2 innate lymphoid cells (ILC2s) with the supernatan
57 was mediated by an increase in the number of type 2 innate lymphoid cells (ILC2s), which released hig
62 2 receptor and drives cytokine production in type 2 innate lymphoid cells (ILCs) (natural helper cell
63 D4(+) T(H)2 cells and the recently described type 2 innate lymphoid cells (ILCs), are targets for IL-
64 l-derived TGF-beta1 displayed a reduction in type 2 innate lymphoid cells (ILCs), resulting in suppre
65 rin mutations have an increased frequency of type 2 innate lymphoid cells in the skin in comparison w
66 that was associated with the recruitment of type 2 innate lymphoid cells/nuocytes and increased TH2-
67 which might be orchestrated by TH2 cells and type 2 innate lymphoid cells though release of IL-33 fro
68 essed epithelial cells; it rapidly activates type 2 innate lymphoid cells to produce IL-13 and IL-5.
70 of IL-33-responsive innate immune cells, the type 2 innate lymphoid cells, was found to produce hallm
71 ting the prompt expansion of IL-13-producing type 2 innate lymphoid cells, whereas IL-25-induced resp
72 ed during tissue injury in sepsis, activates type 2 innate lymphoid cells, which promote polarization
73 to the airways increased lung IL-5-producing type 2 innate lymphoid cells, which required protease-ac
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